2012年10月9日 讯 /生物谷BIOON/ --刊登在10月5日的国际杂志Science上的一篇研究报告中，来自耶鲁大学医学院的研究者揭示了儿科麻醉剂可以帮助压力和抑郁所致的损伤脑细胞进行突触的再生和重新连接。
相比当前别的抗抑郁药物，麻醉剂氯胺酮（Ketamine）可以对全身不同类型的神经递质系统进行作用，理解氯胺酮如何在大脑中工作对于开发新型抗抑郁药物可以提供新的思路和建议，当然这也是数百万慢性抑郁症患者的一大福音。
氯胺酮的快速疗效对于耐药的抑郁症患者来说非常好，氯胺酮的药效可以维持一周至10天，如果大剂量服用该药物可以引发短期的精神异常等病症。
这项研究中，研究者Duman揭示了，氯胺酮可以靶向释放神经递质谷氨酸盐，随后刺激神经元突触的生长，该药物可以逆转由于慢性压力所致的神经元突触损伤。未来研究中，研究者希望通过深入研究，来开发出可以复制氯胺酮疗效的新型药物来治疗抑郁症患者。（生物谷Bioon.com）
编译自：How Ketamine Defeats Chronic Depression
doi:10.1126/science.1222939
PMC:
PMID:
Synaptic Dysfunction in Depression: Potential Therapeutic Targets
Ronald S. Duman*, George K. Aghajanian
Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas. Antidepressants can block or reverse these neuronal deficits, although typical antidepressants have limited efficacy and delayed response times of weeks to months. A notable recent discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants. Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response.
